1. Technical Field
The present application is directed to a composition and method for preventing the formation of plaque and, in particular, to a composition that includes potassium as an antibacterial or an osmotic agent.
2. Related Art
Dental plaque consists of bacterial deposits firmly adhered to teeth. Plaque is neither food or food residue, nor is it just some form of bacteria from the mouth. It is a complex metabolically interconnected, highly organized bacterial system. It consists of dense masses of a large variety of microorganisms embedded in an intermicrobial matrix. In sufficient concentration and with metabolic development, it may disturb the balance of the host-parasite relationship and thereby cause problems such as caries, gingival disease, periodontal disease, and the like. The total counts of microorganisms in dental plaque from the gingival sulcus area have shown the presence of 108 microorganisms/milligram. The intermicrobial matrix is present in only small amounts compared to the large number of microorganisms present. The gingival region of a person with periodontal disease may harbor 200 mgs. of plaque microbiota. This provides an astronomical number of microorganisms that are in contact with gingival tissues. With metabolic development, it can disturb the balance of the host-parasite relationship and thereby cause dental caries, periodontal disease, and mouth odor.
Dental calculus is dental plaque that has undergone mineralization. Bacterial plaque, and calculus continue to form alternatively in layers. Certain oral bacteria are shown to stick to tooth surfaces and to each other by means of extracellular polysaccharides. Both glycans (dextran polysaccharides) and fructans (levans) are synthesized extracellularly by certain bacteria, using sucrose as a substrate. These polysaccharides play an important role in plaque dynamics.
Chronic marginal gingivitis is the most common gingival disease. It is seen in response to the putative bacteria (Acetometacomitans, Gingivales, Bacteroides and others) that are attached to tooth surfaces. The disease may remain stationary for an indefinite period of time, or it may go on to infect and injure the deeper periodontal structures. Gingival disease may be conditioned by systemic factors such as diabetes, hyperthyroidism, pregnancy, puberty, vitamin C deficiency, and it may respond to pathologic agents by gingival enlargement.
Periodontal disease is a destructive inflammatory condition initiated by bacterial plaque accumulation in the gingivo-dental anatomy. “Gingivo-dental anatomy,” as used herein, means the gums and teeth of a subject. It is initially confined to the gingivae, and as it progresses in severity it spreads to involve the deeper periodontal tissues. Inflammation is present in all forms of gingival disease because bacterial plaque, which causes the inflammation, along with local irritational factors that favor plaque accumulation, are present within the gingival enlargement. Plaque induced inflammation gives rise to degenerative, necrotic, and proliferative gingival changes. Atrophy, hyperplasia, and neoplasm can occur in the gingivii.
Pathologic changes accompanying gingivitis are associated with the presence of oral micro-organisms in the gingival sulcus. These organisms synthesize harmful emissions that are capable of causing cellular damage to epithelial and connective tissue cells, collagen, proteoglycans, and glycocalyx (cellular glycoprotein and polysaccharide coat). Widening of the intercellular spaces between junctional epithelial cells in early gingivitis creates a pathway for injurious emissions released by the bacteria to access the connective tissue and penetrate it to sufficiently spread the disease to the deeper tissues.
The first stage of gingival inflammation is vascular dilatation of capillaries which brings forth increased blood flow. Next, gingival erythema may appear due to proliferation of capillary loops between rete pegs. Newly experienced bleeding with probing is an early sign of gingivitis.
In the second stage of chronic gingivitis blood vessels became engorged, and congested, with slow venous return making blood flow sluggish. This results in localized pooling of blood and gingival anoxemia which imparts a bluish hue upon the reddened gingivae. Extravasation of the red blood cells into the connective tissues along with hemoglobin breakdown into the various pigments of bilirubin and hematoidin also deepens the color of chronically inflamed gingivae. Chronic inflammatory gingivae alters the epithelial/connective tissue relationship, pocketing ensues, and color changes are clinically observed. The epithelium proliferates, and rete pegs lengthen downward into the connective tissue. At the same time, the increasing gingival mass of the inflamed connective tissues presses against the overlying epithelium causing it to thin. The engorged blood vessels of the connective tissue extend into the surface epithelium cells, accentuating redness.
With chronic gingivitis and chronic destructive periodontal disease, tissue destruction and tissue repair occur simultaneously. The nature and vitality of the bacteria and the presence or absence of local irritants as related to the strength of one's immune system determine the course of the disease. Persistent local irritants injure the gingivae, prolong inflammation, and cause vascular permeability and exudation. New epithelial and connective tissue cells, collagen fibers, proteoglycans, and blood vessels form even as destructive breakdown affects the gingival color, contour, consistency, size, and surface texture. When increased vascularity, exudation, and tissue degeneration predominate there are marked color changes. On occasion Fibrosis is the main feature with chronic inflammation. In this circumstance the gingivae will have a more normal color.
The putative bacteria that cause periodontal disease are contained in the plaque on the teeth facing the gingival sulci. Their emissions penetrate the periodontal pockets, gingivae, and connective tissues. In addition to direct initiation of the inflammatory response by microbial irritants, periodontal inflammation may be produced indirectly by immunopathologic processes set in action by penetration of microbial antigens into the tissues.
If the periodontal tissue destructive factors are able to outpace the rate of tissue repair, then inflammation exacerbates along with permeability and penetration of the bacterial toxic emissions. The production of new epithelial and connective tissue cells, collagen, proteglycans, along with new blood vessel formation are unable to keep pace with tissue destruction and degeneration of the periodontium. Damage to epithelial and connective tissue cells, collagen, proteoglycans, cellular glycoprotein and polysaccharide coat will ensue, and the disease spreads to the deeper tissues leading to ever more deterioration.
The patent literature is replete with examples of attempts to address problems resulting from plaque and calculus formation. One attempt is disclosed in U.S. Pat. No. 4,585,649 to Lynch dated Apr. 29, 1986, which discloses that various compositions containing monoalkyl and dialkyl ethers of dianhydrohexitols as an essential ingredient are effective in the treatment of oral surfaces and cavities to reduce irritation and plaque accumulation caused by the action of S. Mutans. The compositions of Lynch require 5–95%, by weight, of the dianhydrohexitols. Lynch discloses that the population of S. mutans is drastically reduced in the environment of the dianhydrohexitol derivatives.
Recently, the presence of gum disease amplified by its inflammatory response has been linked to coronary thrombosis. The inflammatory response and the associated high C-reactive protein (CRP) levels released by the liver in human serum provides reason to suspect a higher occurrence of CAD (cardiac arterial disease) among people with periodontal disease when compared with those free-of periodontal disease. Some data confirms that patients suffering from CAD are more likely to have periodontal disease than a comparable population without periodontal disease. Thus, prevention and treatment of periodontal disease may well become a strategy for prevention among patients with risk of coronary artery disease or as a means of secondary prevention for those surviving an acute myocardial infection (AMI).
Inflammation is becoming increasingly recognized for its important role among patients presenting with acute coronary syndromes. High CRP (HsCRP) blood levels and an increasing WBC (white blood count) appear to be a significant predictor of death in myocardial infarctions.
In the opinion of some researchers, infection and inflammation also contributes to atherosclerotic disease.